High Dose Potato Starch Can Make You Fatter, Insulin Resistant By Lowering GLP-1 AND ESPECIALLY If You Are Missing Bifidobacteria longum and Akkermansia mucinophila, aka SAD Microbial Fingerprint (Part V) NSFW

Intrepid gut explorer. Gut Tests Show Depletions of Akkermansia After Long Use of RUMPS, Which Appears to Correlate With Recent Bout 10 Lb Fat Gain/High Blood Sugars/Gout/Fatty Liver:I love gut testing. It shows the gut damage that raw potato starch exerts on the human microbiome because raw starch is not food for humans, but for non-cooking, small brained hamsters and gerbils. Cooked starches are ancestral for humans, but raw are harmful and toxic to both the human host and microbiota.

Tim S. developed Fatty Liver when Bifidobacterium longum and Akkermansia were significantly low compared to that of healthy subjects, 0.12% and 0.0021%, respectively. On every case of pre- and post-raw potato starch, I observe a significant drop of ancestral core microbiota including Akkermansia and Bifidobacterium longum. Neither of these strains ferment starches but Bifidobacterium animalis does. Raw potato starch or HAM (high amylose maize) which are RS2, resistant starch type 2, the kind of starch that humans do not consume because they come from toxic plants and raw materials humans learned to cook or process (with lime/ash) before eating.

These are also the distincut microbial signatures represented of subjects with reported Fatty Liver/ NASH (PubMed):

Like all cases of low Akkermansia on RPS, raw potato starch,, the Folz Family used raw potato starch and experienced also dramatic reductions in Akkermansia with the AMGut stool testing. The Folz family experiment — I briefly reviewed earlier here. Gut diversity dropped in each person on high dose potato starch — particularly for the leanness building gut species.

Child 2 had the least Akkermansia, then high dose potato starch mowed it down to 24-times below normal. Not hard to rebuild: stop RPS, take Akk-building fiber/foods.

Gut Microbe

ANCESTRAL

CORE–

LEAN, GUT PROTECTIVE

MICROBIOTA

uBiome Normal

Avg

Adult1

pre

low-mod

LC paleo

RS3-GOS

beans daily

Adult1

post

4 TB RUMPS

RS3-

diet

Child1 pre

Starches grains, yogurt

semi-

paleo

Child1 post

1 TB RUMPS in water + 1 TSP Psyllium husk

Child2 pre

Child2 post

1 TB RUMPS in water

Akkermansia

(psyllium, inulin-FOS, GOS, yacon, onions, leeks)

1.2%

16.93

1.45

0.24

5-fold below normal

0.26

psyllium

Little change

0.11

11-fold below normal

0.05

24-fold below normal

Tim Steele appears to have had very low levels of the ancestral core microbiota after using raw potato starch for over one year then gradually reported developing several health conditions which are correlated to disease states that are associated with low levels of ancestral microbiota. Several weeks ago, all the contents for this series and the past series (Parts 1-5) were run by and approved by Tim to discuss publicly. I brought up my observations and concerns very early on. He gave his approval to discuss all my concerns, precautions and problems for adverse effects generated by high dosage RS2 including concern for his liver, his high liver tests, SIBO/upper gut dysfunction, recent bout of 10 lb weight gain, gout, and fatty liver/NASH in June 2014, depletions of gut guardians including Akkermansia, and possible connections to the gut obesity fingerprint that is created with high dosage raw potato starch/RS2, the studies, the other N=1s, etc. He’s the only person I know how has taken potato starch for over 1.5 years and his gut profiles are known with major depletions of vital ‘Peacekeepers’ (Faecalibacterium prausnitzii) and other immunoprotective species. Human and animal studies depletions of these gut species predispose to the conditions he developed: carbohydrate sensitivity, fat gain, fatty liver/NASH. Gut researchers have concluded that RS2 (type 2, raw; not cooked RS3) are not prebiotics and do not translate to humans. Metabolic function worsens in human randomized controlled trials.

He is a bold citizen of science and declined the three times that I asked him if he wanted me to omit his data and carbohydrate/fruit related fatty liver/NASH. His liver tests are better. One month ago, his liver test was still 35 and recently he reported it’s now 15. He said “Grace has been privy to all of my gut tests, labs, and health concerns as a friend, not a doctor. I gave her express permission to discuss them how she sees fit. I think that this information needs to be shared freely. If I had a problem with any of this, Grace would be the first to know. I don’t have a problem with her discussing me or my experiments. They are out there for everyone to see and interpret as they wish.”How does the gut microbiota and what we feed it affect our health?Why does diet and dietary additions like supplements change in the composition and function of the gut?How does loss of diversity with a high dosage of a single source of ‘fiber’ adversely affect health?HIGH DOSAGE RAW STARCHES INCREASES BODY FAT IN T2 DIABETES SUBJECTSBodinham et al 2014. Let’s review. High dosage 40 g/day RS2 (high amylose maize) for 12 weeks increased resistance (HOMA) and lowered the fat-burning gut hormone known as GLP1. Post prandially, HAM-RS2 made a tiny spike in GLP1 however longterm it decreased by 33% compared with the control arm (p=0.0049). The drop in the gut hormone GLP1 was quite significant and was one of the few parameters that met statistically significance in this study. Optimal gut health is supposed to yield better fat burning, leanness and metabolic improvements, no? Not high dosage RS2 it appears. Why?I have low gut diversity like most people and for me each time high dose RPS caused problems; it halted fat loss besides giving me reflux and GERD when I took it for over 4weeks. Results Tab 1:–increased fasting TG (p=0.039)–increased LDL cholesterol–increased HOMA% (aka insulin resistance) wtf??!–~35.2% increased pancreas fat wtf? (13.7 v. 10.5, NS)(Body fat depots determined by MRS scanning (n=14).) –increased fat mass (32.2 kg v 31.8 kg)–increased BMI–increased weight–reduced GLP1 (11.4 v. 17.0, p=0.049)–increased IL6 (but lower TNFa)–lower butyrate (p less than 0.001) –lower propionate (p = 0.021)–no improvements in glucose, insulin, Hgba1c

GLP-1 (the Gut-Fatness Hamster Connection)In the Bodinham et al 2014 study, GLP1 was found to significantly decrease by 33% (p=0.049). The well controlled subjects with T2 diabetes also gained on average about a pound of fat in 12 wks compared with the controls. Apparently the researchers examined the fat depots and body fat and found that pancreas fat increased 35.2% on average. Fatty pancreas. Is this synonymous to fatty liver and NASH/NAFLD? The authors don’t clarify or discuss but it is.

The results were unpredicted but if we understand how the gut hormones GLP1 and microbial fingerprint became ‘worse’ on a high dosage non-ancestral ‘fiber’ and diversity was compromised, then it makes sense. Though the stool butyrate decreased, it is obvious there was butyrate in the colon because glucose handling improved a tiny bit. Insulin resistance however tanked as shown by various indicators: increased TG (p=0.039), increased LDL-chol, increased BMI and body fat, and lastly increased HOMA at both the pancreatic beta cells and traditional measurements. Hgba1c and blood sugars didn’t change or improve at all, as the researchers were hoping for. They talk nothing at all about the gut microbiota. Their other study showed the same metabolic disruptions with high dosage RS2.The same thing and worse trends were seen in overweight subjects with high dosage 40 grams daily of HAM-RS2: Bodinham et al 2012Table 1:–increased TG–increased body fat (Tanita bioimpedance scales, 28.1% v. 27.8%, NS)–increased systolic BP (wtf)–increased diastolic BP (wtf)–boatload of insulin increased with 40 g HAM-RS2 acute dosing–increased fasting insulin (88.6 v. 85.4 pmol/L, NS) wtf

Fasting glucose this time decreased but that is because all the spikes in post-prandial insulin is shoving all the glucose into adipose cells now and making them fatty which is clear by the increased TG and higher insulin-related consequences: higher systolic and diastolic blood pressures. wtf. I bet it lowered GLP1 where it is already low and lame in overweight and T2 diabetes subjects.

What is GLP1? I love GLP-1. It helps us to burn and remodel fat. “Glucagon-like peptide 1 (GLP-1), a gut-derived peptide, has been reported to have profound effects on metabolism and to reduce insulin resistance (Yang et al 2013).” High protein diets raise GLP-1 and satiating PYY gut hormones to cause nice fat burning. It appears that high dosage raw starches causes a downward trend of this fat-burning molecule. Ruh-OH. This time it does not depend on either the pre-existing gut or what human gut symbions are missing. It happens in healthy human subjects in several trials so far. Both GLP-1 and GLP-2 are vital for the gut. They seal and heal the gut barrier and much much much more. A healthier barrier leads to healthier leanness and body fat composition because inflammation is reduced.So test your gut, fix your flora and consider the fibers that are (a) ancestral and (b) burn fat by improving metabolic gut pathways and hormones, not potentially worsen them.

The biggest problems I’ve had with RS2 #HAMSTERFOOD is the lack of translation from hamster studies to human. Like statins, RS2 looks beautiful on paper until you dig deeper… look at the downstream consequences… see what it disturbs or benefits. RS2 definitely helps colon butyrate, but what does it do for the upper gut where there is no butyrate? Can it disturb the upper gut flora? How does lowering B longum and Akkermansia affect the host? Does it increase intestinal permeability and inflammation if they are not present? Raw starch RS2 (and artificially produced RS4) in several human studies is associated significant reductions in GLP-1 or lack of improvements (here, here, here). But… not in many rodents………… Boy rodents low raw starches and so do their guts. What about humans? Ruh-OH? Lost in gut translation from hamster to humans? Vastly different gut flora? Bodinham et al 2014 may appear confused but I don’t think so; the authors wrote:

“Animal studies have consistently shown that RS improves glucose and insulin metabolism through increased postprandial GLP1 secretion due to stimulation of the colonic enteroendocrine cells (8, 9). This can result in improved insulin secretion. Most recently our own data has shown restored first-phase insulin secretion in metabolic syndrome (10); however, the lack of translational work has recently been highlighted (11).”

Yesssiree. We are humans, not hamsters. So are our special human gut flora that made us big brained and brilliant fat-burning machines . Our human gut flora eat cooked starches and the whole spectrum fiber. These researchers can see the contradictions, no? As a fiber, high dose RS2 fails to induce fat loss (it appears to raise it) and fails to improve glycemic control and Hgba1c (it in fact worsens fasting insulin and HOMA). On paper, in rodents, high dose RS2 looks decent. (not unlike rabbits + low cholesterol diets + human omnivorous/carnivorous heart disease = animal pharm fallacy)How and why did this poor metabolic outcome occur? Why did raw potato starch and a ‘good gut biome’ not prevent it? Does high dosage potato starch incur a gut profile that is inherently more vulnerable to GERD, reflux, chronic inflammation, and fatty liver/NASH? When high dosage potato starch lowers diversity and Akermansia, Bifidobacteria longum and Christensenella, what are the effects for the host?HUMAN FOOD IMPROVES AND RAISES GLP1Cooked whole beans and beta-glucan/arabinoxylan/RS3-inulin-containing cooked barley (here, here) raise GLP-1 in human trials. Don’t worry, legumes and small seed grains are certainly paleo for many.Non-starchy roots/plants like agave, Jerusalem artichokes/sunchokes, yucca, yacon, endive, and dandelion roots are rich in a special immunoprotective fiber similar to breastmilk (inulin-like oligosaccharides). Inulin-type prebiotics significantly improve GLP-2 in human studies (here). Green vegetables also have small but additive amounts of inulin-oligosaccharides. Inulin is the 2nd most dominant fiber on earth, next to starches.What’s GLP2? GLP-2 is GLP-1’s gut hormone cousin and shown to seal the gut, fix intestinal permeability and lower inflammation.Why are GLP-1 and GLP-2 important? Because the right fiber and combo of fiber modulates and maximizes these gut hormones which basically control our health, body fat storage mechanisms and fat burning metabolism.

VIPER IN SICK GUTS: RPS-RUMPS FFEDS Escherichia coli, an Alcohol Producing Gut FloraAnother problem with high dosage RS2 is what are you feeding and what is one potentially losing? Is RS2 an ‘anti-prebiotic’ meaning does it substantially lower beneficial gut flora that protect and maintain our health and leanness? Does potato-starch-induced reduction or extinction of beneficial flora such as Christensenella, Akkermansia and human-specific Bifidobacteria longum have certain health consequences? I believe so, all the above.E coli is part of the Proteobacteria clade which are overgrowing in several disease microbial fingerprints. We have good non-pathogenic E coli and ‘bad toxic’ adhesive E coli. After antibiotics, more of the ‘bad toxic’ and adhesive, pathogenic E coli are selected. An example of good E coli is the European Nissle 1917 E coli strain. Several gut flora produce alcohol — yeasts, E coli, Clostridium asparagiforme (XIVa), Dorea longicatena (XIVa), to name a few (Duncan, Louis, Flint 2007). The XIVa are part of Lachnospiraceae. These are versatile fermenters and eat both raw and cooked starches. Clostridium and E coli are rapid fermenters of both raw and cooked starches, therefore if they are overgrowing in the upper gut or with triggers (holiday binge-eating, sweets, lack of sleep, etc lol) AND there is a depletion of the gut guardians — what can happen? They will overgrow in the upper gut and produce more alcohol than the body can handle. The alcohol can harden your arteries, pancreas, liver and the brain, and make them appear ‘fatty’.

“Ethanol and acetaldehyde:Microorganisms in the small intestine have the capacity to endogenously produce ethanol which enters the bloodstream and is metabolized in theliver (reviewed in [73]). Indeed, microbial synthesis of ethanol is elevated in obese mice and may play arole in the pathogenesis of fatty liver disease [74].In turn, consumption of ethanol can promote bacterial intestinal overgrowth and has the potentialto alter the composition of the microbiota with an attendant increase in Proteobacteria [73]. Ethanol is proposed to disrupt the barrier integrity of the small intestine, and healthy human volunteers exhibit a transient increase in duodenal permeability following the consumption of alcohol [73,75] with a likely influence upon epithelial tight junctions[73].Microorganisms of the intestine can metabolize ethanol to acetaldehyde through alcohol dehydrogenase(ADH) activity [73]. Acetaldehyde has been shown to significantly disrupt cellular junctions, E-cadherin and to induce profound rearrangement sof actin [76,77]. Certainly, current data suggest arole for the microbiota both in the production and metabolism of ethanol in the small intestinewith a potential impact upon gastrointestinal permeability.” (Joyce, Gahan 2014)

Probiotics and the beneficial flora/guardians in our upper gut work to dramatically lower toxic E coli in every part of the gut (see below green box), particularly the upper gut, aka small intestines (ILEUM) which is the heart of the control center for the immune system — see step #3 on soil and bifido probiotics. (Pubmed) Probiotics like LABs (bifido, lacto) and Akkermansia produce lactic and acetic acids, respectively, which are strongly antimicrobial and antifungal. Soil probiotics (including E coli), LABs, Bifidobacteria longum and Akkermansia line our gut mucosa from where the stomach begins to the end of the rectum and protect the entire gut and modify immunity.

Avoid RPS if there is too much pathogenic E coli. Raw potato starch is a prebiotic for pathogenic E coli. This Russian researcher states RPS are ‘prebiotics for E coli (Ivchenko et al 2006).’ (the good and the bad strains).

Intrepid gut explorer. Gut Tests Show Depletions of Akkermansia After Long Use of RUMPS, Which Appears to Correlate With Recent Bout 10 Lb Fat Gain/High Blood Sugars/Gout/Fatty Liver:I love Tim S. and his intrepid gut testing. Several weeks ago, all the contents for this series and the past series (Parts 1-5) were run by and approved by Tim to discuss publicly. I brought up my observations and concerns very early on. He gave his approval to discuss all my concerns, precautions and problems for adverse effects generated by high dosage RS2 including concern for his liver, his high liver tests, SIBO/upper gut dysfunction, recent bout of fatty liver/NASH in June 2014, depletions of gut guardians including Akkermansia, and possible connections to the gut obesity fingerprint that is created with high dosage raw potato starch/RS2, the studies, the other N=1s, etc.

He is a bold citizen of science and declined the three times that I asked him if he wanted me to omit his data and fatty liver/NASH. His liver tests are better. One month ago, his liver test was still 35 and recently he reported it’s now 15. He said “Grace has been privy to all of my gut tests, labs, and health concerns as a friend, not a doctor. I gave her express permission to discuss them how she sees fit. I think that this information needs to be shared freely. If I had a problem with any of this, Grace would be the first to know. I don’t have a problem with her discussing me or my experiments. They are out there for everyone to see and interpret as they wish.”My potato-starch induced GERD With RUMPS: Recently I had GERD/reflux after several weeks of 20-40 grams RPS, raw potato starch. Several other people have reported this too. I was previously using Version B (inulin + acacia) and psyllium and had fantastic gut results such as the best flattest tummy in 7 to 8 years and improved digestion and gut health. I gave the RPS one last try and initially no problems that I had had earlier (immunosuppression). Tim S. had also had GERD last winter on sedentary days and didn’t think much of it until I had reflux myself. In the past, I’ve never had reflux except a couple times after drinking pots of coffee or when I was pregnant in the 3rd trimester. Reflux was super annoying but fortunately went away with resuming probiotics (bifido/lacto and soil) and taking some gut support (ACV, enzymes, etc) temporarily. Besides RPS, I think no B longum was a factor; I had stopped the B longum supplements several months earlier and never resumed. Stress from moving from Shanghai back to USA likely lowered the bifido and lacto more than I had thought. Potato starch lowers the populations of non-starch eating bifido which make up huge portions of our fecal and mucosa-associated bifido microbiota (see prior post).In healthy controls, Bifidobacteria longum is a gut specialist and found in the majority:B longum 43.5%B pseudocatenulatum 8%B bifidum 6%B dentium 1.5%

Recently what made me rethink the downstream effects of high dosage potato starch was how Tim S. had a bout of fatty liver again this past summer, after over one year and a half on high dosage potato starch — high liver functions tests, tender and painful liver on touching, gained body fat and took several months for the ALT, AST to reduce to normal again.

RPS (RAW POTATO STARCH) = BLOCKER OF FAT BURNING?After several citizen science N=1 experiments, we can observe now how high dosage potato starch may re-inforce these ‘chronic illness’ gut profiles by its anti-prebiotic effects where it lowers beneficial flora in the gut that are integral and vital for protecting the upper gut from pathogens like E coli and other alcohol producers, increases leanness, GLP1, revving up fat burning and carbohydrate metabolism:–Christensenella –Bifidobacteria longum –Akkermansia (see prior post: high dosage raw potato starch tanks Akkermansia)

What is curious to me is that scientists can restore and alleviate fatty livers and intestinal permeability by giving live probiotics of Akkermania to rodent models (Everard et al 2013). By giving prebiotics (FOS) to fatty liver/diabetes/obesity rodent models, reversal of all the hallmark biomarkers of these conditions rapidly occurs. Restoration and reversal of intestinal permeability happens, LPS decreases, metabolic endotoxemia reverses, inflammatory markers reduce, and insulin/blood sugars normalize.

“For instance, a decrease in Akkermansia muciniphila causes a thinner intestinal mucus layer and promotes gut permeability, which allows the leakage of bacterial components. Interventions to increase Akkermansia muciniphila improve the metabolic parameters in obesity and NAFLD. In children, the levels of Escherichia were significantly increased in nonalcoholic steatohepatitis (NASH) compared with those in obese control. Escherichia can produce ethanol, which promotes gut permeability. Thus, normalization of gut microbiota using probiotics or prebiotics is a promising treatment option for NAFLD.” (Miura et al 2014)

VERY DIFFERENT FROM HUMAN BODINHAM ET AL 2012 and 2014 STUDIESBodinham and other studies fail to account for the gut microbiota effects of the ‘fiber’ that they are studying and the metabolic consequences. That’s too bad. We are what we eat and our health is determined by our gut microbiome. We can shift and shape this, and we and the researchers are doing it all the time now. In several human studies, body fat (‘fat mass’) and upper gut permeability significantly improve with FOS and inulin-type fructans. The obese subjects in the below trial were never diagnosed with fatty liver, but with intervention with inulin-FOS, weight, BMI, insulin resistance, butyrate, SCFA and LPS/endotoxemia (proxy for permeability) and other metabolic parameters all improved. Per personal communication with one of the researchers, as can be predicted, Akkermansia significantly increased in the below trial.

“The species Bifidobacterium longum, Bifidobacterium pseudocatenulatum and Bifidobacterium adolescentis were significantly increased at the end of the treatment in the prebiotic group (p less than 0.01) with being B. longum negatively correlated with serum lipopolysaccharide (LPS) endotoxin (p less than 0.01). Total SCFA, acetate and propionate, that positively correlated with BMI, fasting insulinemia and homeostasis model assessment (HOMA) (p less than 0.05), were significantly lower in prebiotic than in placebo group after the treatment period.”

FATTY LIVER REVERSAL WITH OLIGOSACCHARIDE-RICH YACON SYRUPYacon is an ancestral non-starchy root. It can be boiled down and produce a nice syrup which has little energy for humans but fiber and prebiotics for our gut flora including Akkermansia and Bifidobacteria longum. Oligosaccharides in whole foods (see below) and yacon help boost the species lost by high-dosage-raw-potato-starch. The game-changers: Akkermansia and B longum specifically.The Folz family experiment — I briefly reviewed earlier here. Gut diversity dropped in each person on high dose potato starch — particularly for the leanness building gut species.

Child 2 had the least Akkermansia, then high dose potato starch mowed it down to 24-times below normal. Not hard to rebuild: stop RPS, take Akk-building fiber/foods.

REVERSAL OF LIVER TESTS/FATTY LIVER WITH STOPPING RPS AND TAKING YACONRecently my buddy Justin told me he stopped potato starch (no changes) after a few weeks, then took yacon syrup for 2months.He was surprised to see his high liver tests (fatty liver) ALT improved from 50 to 26 and AST to as low as 23 (healthy optimal levels less than 15 (male); less than 12 (female). Thanks Justin!@Gut_Goddess ALT 50–>26, ALP 101–>66, AST–>23. Getting there.

Everyone appears to have low B longum and Akkermansia which are risk factors for chronic inflammation according to new human gut microbiota. Studies show their replenishment yields many health benefits and control of inflammation and disease. If you don’t have FODMAP intolerances, consider both Version A and B of bionic fiber in the 7 Steps to rebuild these.

“A. muciniphila is important for a healthy host as its decreased abundance is associated with compromised health including acute appendicitis, ulcerative colitis, autism and atopic diseases. Finally, the abundance of A. muciniphila is inversely correlated with obesity …plays a pivotal role in obesity as its duodenal delivery regulates fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance”Source

It’s known ethanol amplifies insulin secretion, driving down blood sugar rapidly called Reactive Hypoglycemia where hypoglycemia is associated with mental imbalances including depression, epilepsy, etc. So, beware the spiked egg nog or risk hypoglycemic hangover. You may have added ethanol-producing E. coli or other proteus associated with dementia and rheumatoid arthritis in urinary tract infection. I tend to believe adhesive E. coli as cause of PCOS and endometriosis where bee propolis appears useful in ameliorating adherence. And to all a good night.

Nice synopsis. Adhesive E coli is implicated also in PCOS, infertility, frailty in elderly, colorectal cancer, IBD-Crohns and many other conditions like breast cancer.

Have you heard of persorption? Gut Leakiness allows starch granules to enter the blood stream. Unless the gut and body gets seeded by beneficial flora and probiotics, then e coli that is pathogenic and adhesive will thrive with the wrong foods and potato starch. I think this is partly what occurred in the overweight and T2D Bodinham trials.

There is a timeline for optimal health recovery — worsening the microbial fingerprint actually will exacerbate SIBO conditions as seen in the Russian pig study where 14% RPS was given and then the ETEC E coli overgrew in the small intestine/ileum, colon and feces.

Not good for optimal health or LEANNESS lol

Anonymous

When RUMPS is cooked, does it lose its rs2 permanently, regardless if it’s cooled again or not? Thank you!

Yes. Once it becomes RS3 it is more accessible for a great majority of the gut flora to degrade and eat. Many more can get energy and fuel from RS3 compared with RS2 which is in hard granules that only more primordial bottom feeders can access.

RS3 feeds lactobacillus which is a beneficial symbiont in the upper gut that RS2 fails to feed

What about people tryin to lower insulin and improve metabolism? Mmmhhh

Anonymous

Dr. BG, is there a perfect mix of these prebiotics that would help slowly crowd out over time the harmful bacteria? maybe a company like Bob’s Red Mill would be interested in your expertise on the subject and would put out a line of inexpensive fiber mixes that the avg person can afford. seems like several different fibers would be much more beneficial to gut health than just potato starch.

So domino, if you have no desire to help, then just leave us lowly laymen be in our ignorance. You are annoying me.

Anonymous

Speaking of Charts/Tables could you write an article that lays out the different supplemental pre-biotics and the contraindications and indications for using them. I.e. that visually clarifies when you should and shouldn’t use them, how you could test and trial each one’s suitability for yourself. E.g. I have had some blood in my poo for a couple of days and I:1) Took a round of antibiotics for a middle ear infection a month ago. I have followed up with lost of probiotics 2) Stopped RPS about three weeks ago and added in inulin and psyllium 3)Have a family history of piles 4)Ate a lot of floury products for birthday and Xmas and I usually abstain. I plan to be very disciplined for a while regarding no sugar and flour/grain, and today I have dropped the psyllium for now. I have ordered some acacia powder. Any suggestions?

The rest of us see through your heckling. If you have not had any problems with RPS, then I’m happy for you. But I’m here because I have had serious issues with RPS as have many others. Don’t you have something better to do?

Sincerely,MsMac

Anonymous

Hi Grace, I hope you didn’t think I was having a go last night when I raised the issue of my tummy troubles. It was more of a rambling on about how did I get here. My stomach is feeling tender and reactive to eating. The trouble for me is that I have made too many changes all at once, including eating stuff I haven’t for quite a while like cakes and biscuits, and bread crumbed risooto (made with wheat flour) for a friend’s birthday and for Xmas (pudding etc., plus hitting the ham pretty hard. Maybe I have created a problem from previous use of RPS. Maybe I am more sensitive to the wheat/grain stuff than I used to be. I mean I did go off the RPS and onto the inulin and pysllium thrre weels ago, but I also had anitbiotics a month ago, added in Bee Pollen, stopped drinking coffee, upped the salads, and had the grain based breakout. You have said yourself some people don’t do so well on psyllium. I have created my own situation of too many variables, so I have to go back to basics and start again. Cheers, Adrian. PS It wasn’t me who said you were nasty but I was a bit taken aback by your response.

Awe, yes, such clever bastards!! You must be mighty proud of your heckling expertise.

Anonymous

Hi Grace, I am not sure if MsMac is referring to me but if she is she is wrong. Anyway, I just realised I have been using a anti-inflammatory pain relief gel for my recovering knee injuries which I started a few days ago. I didn’t think of it because it is a topical gel and not a tablet form. I just looked it up and side-effects include:bloody or tarry stoolsupper stomach painmild nausea, stomach pain, upset stomach. Maybe this is the actual problem. Cheers, Adrian

DR. BG – do you have suggestions for raising F. Prausnitzii?? I would LOVE to take a probiotic of it. From what I’ve read online it’s too hard to capture and keep alive in probiotic form. Any suggestions? Seems like a very useful one.

“AXD feeding resulted in a higher number of Faecalibacterium prausnitzii, Roseburia intestinalis, Blautia coccoides-Eubacterium rectale, Bifidobacterium spp. and Lactobacillus spp. in the faeces sampled at week 3 of the experimental period (P< 0·05). In the caecum, proximal and mid colon, AXD feeding resulted in a 3- to 5-fold higher pool size of butyrate compared with WSD feeding, with the RSD being intermediate (P <0·001).”

AG was associated with a statistically significant increase in the concentration of total bacteria, Bacteroidetes, Faecalibacterium prausnitzii, a delayed bifidogenic effect and a decrease of the pathogenic Clostridium perfringens. FOS led to a strong lactobacillogenic effect.

Anonymous

Another brilliant Post Grace. Kicking A!S and Taking Canes.

James N.

Dr BG,

This has been a very helpful post. The numbers are what they are and it appears that raw unmodified potato starch hammers the gut guardians (or gut repair?) bugs that are required for a healthy gut. I did find it interesting that beans appear to boost Akkermansia; a gut guardian, if present. This suggests to me that properly prepared non-toxic legumes (beans) may in fact be Paleo. It would be interesting to know if there are any other foods that boost the gut guardians, as well.

Dr. BG – Thanks for posting the info about arabinogalactans. I ordered some. I think they’re be great for my gut. BUT I have Multiple Sclerosis, and apparently there’s an immune modulating component to the AG that may actually be dangerous for people with MS. This might be an advantage or a disadvantage. I saw on WebMD that you should take AG if you have MS, but there’s a study suggesting it has positive impact on people with MS. It seems like nobody knows for sure what interaction it’s going to have. Any insight on that you might have would be welcome. Probably ought to talk to a doctor when I find one.

Aaron, depending on current gut balance, it seems possible AG might feed overgrowth where microbes stimulate autoimmunity. That’s why stool testing seems so important or we risk shooting in the dark. You may find this recent MS paper including its references helpful:“an increased understanding of the regulation of tight junctions at the blood-brain barrier and in the intestinal wall may be crucial for design of future innovative therapies . . . Taken together, we report the novel finding of a “leaky gut” syndrome including zonulin upregulation in the EAE animal model for human MS. Recent reports showing that IBD patients are at higher risk for MS, while the course of the IBD disease is not influenced by the MS [8], [9], is further supporting a key role of the gut in the modulation of CNS autoimmunity.”http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0106335

Along the same line, I’ve wondered if psyllium can feed prevotella overgrowth associated with type 2 diabetes.

Thanks for your email, will respond soon. Getting a gut profile done will yield much for you. What do you think of Terry Wahl’s approach and detoxification programs?

Keith!

Psyllium usually works for obese and diabetics because the viscosity and binding benefits outweigh potential risks to Prevotella overgrowths.

Psyllium (AX and AXOS) selectively feed B longum, the superstar of the gut mucosa for the entire GI tract.

Obes Rev. 2012 Nov;13(11):1034-47. doi: 10.1111/j.1467-789X.2012.01020.x. Epub 2012 Aug 5.Effects of psyllium on metabolic syndrome risk factors.Pal S1, Radavelli-Bagatini S.Author informationAbstractHigh-fibre intake has been shown to reduce the risk of metabolic syndrome (MS), cardiovascular disease and type 2 diabetes. Psyllium is one of the most widely used fibre supplements because it is reasonably cheap and is better tolerated than other fibre supplements. The review of the literature supports the notion that the consumption of psyllium provides benefits to many components of the MS. Psyllium supplementation does improve glucose levels and insulin response, blood pressure, as well as lipid profile in both animals and humans, thereby reducing metabolic risk factors. Appetite has also been reported to decrease after the consumption of psyllium in most studies. Collectively, psyllium supplementation could be promoted to patients who present MS risk factors, such as hypercholesterolaemia, hypertriglyceridaemia and hyperglycaemia. It may also play a role in controlling body weight, body composition, appetite and hypertension, but further investigation is still required.

Great post on fibers to feed Akkermansia and Bifidobacteria longum. Do you have any thoughts on dietary fats and their role in feeding or harming the good bugs? Are the populations levels of good bugs the primary way to test for intestinal inflammation or are there other biomarkers to test. I have read some mouse studies but would like to translate those observations to human needs.

James N.

It looks like asparagus is another food that is high in inulin and feeds the bifidobacteria. The below listed article says that asparagus is 5% lower in inulin than chicory root.

It’s awesome — many green vegetables also have inulin but not as high as artichokes or asparagus or dandelion (stems-roots). Root vegetables have amazing prebiotics that bulk stools and increase the microbial masses in our guts — for all of our flora like Akk, B longum and (I suspect) Christensenella. Don’t forget to incorporate non-starchy tubers such as rutabagas, parsnips, daikon, onions, fennel, etc

DoggermsGreat question!~ I think macronutrients are more important but fats do count if high enough dosages on the gut flora. Lauric acid is wonderful to shift out protozoa and some pathogens; it doesn’t reach all of them. Olive oil and its polyphenols appears to have wonderful effects also on the gut.

Anonymous

We’re trying to heal leaky gut and candida via a standard paleo approach but after reading your post and related studies, wondering about the validity of adding things like beans and oats back into the diet. No one in our family experiences any digestive distress eating beans, or other FODMAPS for that matter. But just about every “protocol” for gut healing,takes out these foods. Interesting…

I came to your blog via a Google hit on vitamin d roid rage, then checked this, your (same person?) latest post. Nice blog, but why are you writing about raw potato starch (RPS)? Who eats that? If I eat a well cooked purple sweet potato, are you suggesting I’m consuming RPS?

I wonder, if there is any possibility that a table can be made where column 1 mentions the kind of bugs, column 2 mentions stuff that they feed on, be it fiber or resistant starch and column 3 lists the stuff that reduces their numbers.

If you can add a rough product suggestions, that would be great. For e.g. after noticing your table about inulin and RS3, I quickly checked Chicory root powder and all I find is, roasted variety. The 5 posts that I read didn’t mention if it should be roasted or not roasted. Will remove ambiguity.

Last question,This is of important to me as my son has autism and I am trying to modulate his gut flora. With preliminary interventions I did, I am noticing success so I would like to increase or decrease some bugs with precise accuracy (to check how/if they change symptoms). DS has Prevotella that you mentioned in ASD gut. Any idea how they can be reduced?

Thanks a lot in advanceand thanks again for these great posts. I am going to take some time to imbibe 7 years of your work.

Raw potato starch selectively feeds bacteroides, prevotella, E coli, enterobacter, and clostridium — which are all often high in ASD and other conditions — every western civ disease! So I would avoid.

COoked RS3-rich sources on the other hand are rich in inulin, oligo, arabinoxylan, pectins and other prebiotics which feed the gut guardians which eliminate the toxic strains of all the above I listed.

What if you are FODMAP sensitive? Can you take the bionic fiber with inulin? I saw results with the old recipe that had PS + Psyllium + ORAC + SBO. Should I switch to the new inulin recipe? Trying to get rid of my skin issues.

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